Are you looking for a way to inexpensively get those pesky fleas under control without having to go to the vet for a prescription for expensive flea control or heartworm / flea control?
1) Treat you house with flea bombs available from Kroger and other retail home supply stores.
2) Treat your carpets, furniture and all areas where your pet lives with Fleabusters - available at Amazon: http://www.amazon.com/Fleabusters-Rx-Fleas-Plus/dp/B000MS6Q2Q/ref=sr_1_1?ie=UTF8&qid=1370692080&sr=8-1&keywords=flea+busters
3) Treat your pets once weekly for 3 weeks with Capstar available from you Kroger pharmacy and online at Amazon. Capstar works for only a short period but kills all the fleas on your pet.
If you effectively treat your home and kill all the fleas on your pet you have eliminated the flea problem for your pet. It is important to continue to treat your house every 3-4 months for a year to kill any fleas emerging from the cocoon stage in which they are virtually indestructible
For added protection add over the counter once monthly flea prevention like Frontline or Pronyl; both available at Kroger.
A torn cranial cruciate ligament, commonly known as an ACL tear in human medicine, is one of the most common injuries in dogs. More than one million CCL repair surgeries are performed annually. In 2003, owners spent $1.32 billion on knee surgeries and related care. Here at Vets Helping Pets, the veterinarians diagnose and care for your pets’ knees. Diagnosis is a combination of physical exam and radiographs. After diagnosis, we will discuss treatment options. Following a cranial cruciate ligament tear, no treatment method is one hundred percent effective, and the knee will never be the same as a non damaged knee.
Dogs tear their cruciate ligaments from a combination of factors. It is rarely a single trauma. Current consensus is that CCL tears are caused by a combination of factors: body type, excess weight, and heritable traits. Dogs who tear one CCL are at a significant risk to tear the opposite side.
According to recent studies, approximately sixty percent of dogs will return to adequate function with conservative management: weight control, physical therapy, and anti-inflammatory drugs as needed. For the remaining forty percent, surgery will be needed for a successful outcome. There are numerous different surgical options available, and none have been proven to provide consistently superior results. Here at Baker House we use a lateral stabilization technique.This involves opening your pet’s knee, visualizing meniscal damage, removing the meniscus if necessary, and placing heavy nylon suture outside of the joint capsule anchored to the tibial crest and and the fabella that temporarily stabilizes the joint. This suture is securely crimped down, stopping the forward motion of the tibia, known as a cranial drawer. It’s this motion and instability that causes the arthritis and pain. This suture will eventually break, but by that time the knee will have scarred to provide stability.
Currently the other technique most commonly used is a tibial plateau leveling osteotomy. When this technique was first developed, it was believed that an excessively steep angle between the tibia and the femur was a contributing factor for ruptured CCL’s. This has sense been proven incorrect, and there is no evidence that a TPLO provides a superior outcome, and it has several potential disadvantages. A TPLO is significantly more expensive as it requires special instrumentation and plates. All surgeries have a potential for complications, and the overall complication rate for the two procedures is similar, however a TPLO has a potential for catastrophic failure resulting in amputation.
If you believe your pet has ruptured a CCL, the veterinarians at Vets Helping Pets are happy to provide a second opinion and discuss treatment options.
Babesiosis is another blood disease caused by a parasite (this time a protozoan) carried by several species of infected ticks.
Symptoms can range from anemia and skin blotches to uncontrollable bleeding and shock. Fever and poor condition are common.
Babesiosis can be diagnosed by clinical signs and history, direct examination of the blood, or titration of a blood sample.
Babesiosis is a disease known around the world. It is caused by a protozoan that parasitizes red blood cells of domestic and wild animals, and occasionally people. The organism is transmitted to a host by the bite of infected Ixodid ticks such as the brown dog tick and black-legged tick. Various other tick species have also been incriminated.
The major financial impact of babesiosis is on the cattle industry (B. bigemina and B. bovis) but infections in humans and dogs are becoming a concern. Two species of the parasite are found in U.S. dogs: Babesia canis and B. gibsoni. In the United States, the disease is most prevalent in the southeast, but pockets of infection exist in the northeastern states as well. Cats also can be infected with Babesia organisms (B. felis, B. cati, B. pantherae, B. herpailura), but these organisms are reportedly not present in the United States.
Humans have been infected with Babesia canis, but only rarely. Most commonly, infections in humans occur due to Babesia microti, which is transmitted by the deer tick, I. scapularis. Numerous cases have been documented, including co-infection with Borrelia burgdorferi and Babesia microti in people living in Massachusetts and Connecticut.
When an infected tick bites, the Babesia protozoa enter the host's red blood cells. Babesia organisms begin to multiply. As a result of the host immune system's attempt to eliminate the organism, and because of the organism itself, anemia often results. Young dogs are most susceptible to infection. If heavily parasitized, they can present in a severe state of hemorrhagic shock.
Less dramatic but equally serious, dogs can show a state called disseminated intravascular coagulation (DIC), in which platelet numbers have dwindled sharply and small hemorrhages have developed in the skin and mucous membranes. A dog with chronic disease typically shows signs of fever, loss of appetite, and poor body condition. If diagnosis of disease is not made by history and clinical signs alone, the organism can be detected in a sample of blood from the capillaries of the ear or tail tip which has been smeared onto a slide and treated with Giemsa stain. Titers can be assessed by immunofluorescence. If titers are greater than 1:80, a positive diagnosis can usually be made.
Diminazen aceturate and imidicarb dipropionate are the two most widely used drugs to treat babesiosis. Long-acting tetracyclines reduce the severity of disease if treatment is started early. Supportive therapy may include intravenous fluids and blood transfusions.
Many tick species can spread tick paralysis.
Ticks vary in neurotoxic capabilities, so no one knows how many are needed to induce paralysis. In some cases, it has been as few as two ticks.
Sometimes, the tick itself is the causative agent of disease. In addition to transmitting many pathogens, some tick species secrete noxious substances capable of causing disabling or lethal toxic conditions, termed toxicoses, in their vertebrate hosts.
The best known of these toxicoses is tick paralysis, which is an ascending motor paralysis generally assumed to be induced by substances introduced into the host with the saliva when the ticks attach and feed. Tick paralysis is relatively common in livestock and pets, causing injury or death to thousands of animals each year. Cases also occur in humans and may lead to death if the attached tick is not removed.
In North America, tick paralysis in humans and domestic animals has been reported most frequently from British Columbia and in areas of Montana, Idaho and Washington near the Canadian border.
Many tick species are important as the causative agents of tick paralysis in different parts of the world. In North America, they are Dermacentor andersoni and Dermacentor variabilis, as well as Amblyomma americanum. (The genus Dermacentor is a large one, with many members that have been implicated not just in the spread of tick paralysis, but also ehrlichiosis and other diseases.)
The predominant symptom in tick paralysis is disruption of motor coordination. After a brief (5 - 7 day) incubation period, paralytic symptoms appear while the tick is still attached. Paralysis affects the lower extremities first and gradually ascends through the body. Paralysis of chest muscles leads to death from respiratory failure. In most cases, removal of the attached tick (or ticks) terminates the condition and allows for a complete recovery.
For unknown reasons, only certain individuals in the population of paralysis-causing ticks are capable of being neurotoxic, even in species that are notorious for causing the disease. Perhaps for this reason, data on the number of ticks needed to induce paralysis are ambiguous. Studies of D. andersoni show that as few as two female ticks were sufficient to induce paralysis in young puppies; larger numbers were required for paralysis in larger animals. Tick paralysis is actually only one expression of a continuum of toxicoses that may result from tick parasitism. Tick bites also may cause allergic hypersensitivity and toxemias. Toxic reactions to tick bites have been known for many years. In contrast to tick paralysis, toxic reactions develop within a few hours.
Many other tick-borne diseases of medical significance are also known to exist. These include tularemia, Q fever, and others. Specifics of these diseases, which are less common in North America, are intentionally omitted in this cours
Rocky Mountain spotted fever is still another infectious disease caused by rickettsia carried by ticks.
These rickettsia damage blood vessels, causing blotchy skin (the "spots" in RMSF) and even hemorrhage.
RMSF can mimic other tick diseases. Definitive diagnosis usually depends on antibody titers.
Rocky Mountain spotted fever (RMSF) is another tick-borne disease that affects small mammals, dogs, and humans. The infectious organism is called Rickettsia rickettsii. This rickettsia is most often transmitted by the American dog tick (Dermacentor variabilis) or the Rocky Mountain wood tick (D. andersoni), and less commonly, by the lone star tick (Amblyomma americanum).
Rocky Mountain spotted fever can be transmitted to humans during the removal of an engorged tick from a pet. If the tick's midgut and excrement get into a person's eye or abraded skin, infection is possible. Clinical signs early in the disease process consist of high fever (up to 105° F), loss of appetite, swollen lymph nodes, and sore joints. The severity of disease depends on the magnitude of infection, which can vary.
The rickettsial organisms enter the endothelial (inner cell) lining of small blood vessels and reproduce. Damage to this inner lining of blood vessels, along with a loss of platelets, can lead to the development of petechiae (minute reddish/purplish spots in the skin or mucous membranes containing blood) and ecchymoses, (blotches in the skin and mucous membranes due to the escape of blood from ruptured blood vessels). A disorder called disseminated intravascular coagulation (DIC) can develop in extreme cases, which leads to epistaxis (bloody nose) and uncontrollable hemorrhage. Rocky Mountain spotted fever can mimic other diseases such as Lyme disease and ehrlichiosis due to the development of lameness and fever.
Despite its name, most of the cases of Rocky Mountain spotted fever occur east of the Mississippi River. Diagnosis is made by demonstrating a four-fold increase in antibody titers in conjunction with the above clinical signs. In the western United States, a single titer of 1:128 or above suggests recent infection. In the eastern United States, a single titer of more than 1:512 is required to signify active disease. Regional strain differences among R. rickettsii organisms are responsible for these differing titer cut-offs.
Treatment with tetracycline antibiotics is usually very effective. Additional supportive treatment with intravenous fluids and blood transfusions may be necessary. Immunity appears to be lifelon
Ehrlichiosis is another infectious disease spread by ticks. Infection with Ehrlichia can cause chronic debilitating disease and can be contracted by both dogs and humans. This parasite is a rickettsia, a microorganism similar to bacteria. The organisms that cause ehrlichiosis have been reclassified into ehrlichias, anaplasma and neorickettsia. The term ehrlichiosis will probably continue to be used, but is no longer technically correct.
Canine ehrlichiosis first gained attention as a significant disease during the Vietnam War, causing the death of hundreds of military dogs overseas and chronically infecting many that returned to the U.S. (For this reason, among its many names, it is sometimes called "tracker dog disease.") It has now been reported to occur on four continents: Asia, Africa, Europe, and North America. Serologically confirmed cases have been recorded in most states of the United States.
Ehrlichia canis is the causative organism in most clinical cases of canine disease (but occasionally other strains of the organism have been found). The primary vector responsible is the brown dog tick, Rhipicephalus sanguineus. Larvae, nymphs and adults are all able to transmit the disease. It has been shown that ticks can survive up to 568 days as unfed adults, and can transmit infection for 155 days after becoming infected. This phenomenon allows ticks to over-winter and infect definitive hosts the following spring.
There are three phases to the disease in companion animals (most commonly the dog). In the acute stage, the organisms multiply and spread throughout the body. Common clinical signs include fever, ocular (eye) and nasal discharge, loss of appetite, weight loss and swollen lymph nodes. In some dogs, the clinical signs may be mild and non-specific. In other cases, they may be severe and life-threatening, including hemorrhages and convulsions. This stage may last two to four weeks.
A subclinical stage follows the acute stage. Now the organism is present but not causing any sign of disease. Animals improve clinically and antibody levels begin to rise. (If the animal passed through the acute phase without its owner being aware of the infection, the dog may enter this phase showing laboratory changes but no apparent signs of illness.) During this stage, the dog or cat may recover. However, it remains susceptible to reinfection.
If the animal cannot eliminate the Ehrlichia organism, the chronic stage ensues. Some animals may become carriers of the disease for months or years. As such, they can be sources of infection through ticks that feed upon them.
The chronic phase of this disease may be characterized by mild signs, but more often involves severe illness. Blood disorders are common, including decreased bone marrow production of blood cells, leading to anemia, increased susceptibility to infection, and bleeding tendencies. In cases of severe hemorrhage or anemia, transfusions of whole blood or plasma may be needed.
The prognosis for an animal's recovery mostly depends on how early in the course of the disease the treatment is begun. Antibiotics such as tetracycline, doxcycline and chloramphenicol are frequently effective in the treatment of ehrlichiosis in dogs and cats if given during the acute phase, but sometimes not effective at all during the chronic phase. Some newer research indicates that certain dogs may need to be treated for up to 4 months.
People are also susceptible to ehrlichiosis, but because tick bites are required for transmission, the disease cannot be spread directly from dogs to humans. Rather, infected dogs serve as sentinels, indicating the presence of infected ticks in the area. They also may be a source of the organism for either ticks that may infect humans or other dogs.
Clearly, preventing ehrlichiosis is a better course than simply trying to treat it. Controlling tick infestation is the most effective means available to us.
Lyme disease in people is now the most common vector-borne disease in the United States, with over 153,000 cases reported to the Centers for Disease Control (CDC) by 49 states and the District of Columbia between 1993 and 2002. Lyme disease has been documented in every state in the United States except Montana, but there are distinct areas that are considered more endemic than others. These include the Northeast and mid-Atlantic coast (MA, RI, NY, NJ, PA, MD, DE, CT), the upper Midwest (MN, WI), and the Northwest (CA).
Since the early 1990s, Lyme disease in dogs has been the focus of much research relating to the origin, treatment, and prevention of infection. The causative agent is a corkscrew-shaped spirochete named Borrelia burgdorferi. This bacterial organism is transmitted primarily by nymphal ticks of Ixodes scapularis (black-legged or deer tick) between May and July in the Northern Hemisphere.
It is reported, however, that only approximately 5-10% of infected dogs develop overt clinical signs after infection with the causative agent, B. burgodorferi. However, it is clear that dogs can become infected with B. burgdorferi after being infested with I. scapularis ticks. They develop joint disease and mild to moderate arthritis in more than one joint, whether they become symptomatic or not.
Furthermore, treatments for Lyme disease in dogs can have mixed success. Antimicrobial therapy with tetracycline, doxcycline, chloramphenicol, or antibiotics like cephalosporins for 10 to 30 days is believed to be effective in treating Lyme disease in dogs, and lack of response after three days of antibiotic usage is considered to be cause for reevaluation of the diagnosis. However, it has been proven that dogs can become persistently (chronically) infected after natural tick challenge exposure with B. burgdorferi, despite prolonged courses of antibiotic therapy.
Because Borrelia organisms can persist for many months despite treatment, preventing Lyme disease through vaccination and reduction in tick numbers is the most logical approach.
Definition of OCD
The symptoms are lameness in the affected limb. Some dogs have a barely noticeable limp and others are unable to bear any weight on the leg. The lameness tends to worsen after periods of exercise and improves after rest.
Seventy four percent of the cases of OCD occur in the shoulder joint, 11% in the elbow, and 4% in the hock. When it affects the front shoulder, a shortened forelimb stride may be noted due to reluctance to flex and extend the shoulder joint. Occasionally, the disease will affect both limbs simultaneously and the dog may be reluctant to move.
Noticeable Symptoms Include:
Diagnosis is based on history, physical exam, and radiographs
(x-rays) can be easily done at Baker House Animal Hospital. On physical
exam, we notice joint pain. For instance, most healthy dogs show no
resistance when their shoulder joint is fully flexed and extended.
However, if they have an OCD lesion in their shoulder, they may resist
shoulder manipulation and may even cry out in pain when it is
attempted. In addition, this flexion and extension of the shoulder
joint may worsen the lameness.
Radiographs of the affected joint are taken to confirm the diagnosis. The dog is often sedated so that full relaxation of the joint can be obtained. Several views of the affected joint and the healthy joint on the other side are taken for comparison. The separations of the cartilage or joint mice are often identified on radiographs.
Causes of OCDThe cause of OCD is considered to be multifactorial. Here are some of the known causes of OCD:
Trauma, whether chronic or acute, may contribute to the formation of OCD lesions. Injury to the surface cartilage may lead to the separation of the cartilage from the bone or cause a decrease in blood supply that leads to cartilage flap formation.
It appears that there is a hereditary link between parents and offspring and the formation of the disease. Certain breeds and genetic lines are much more likely to develop the disease. Careful screening of parents against this disease is recommended during the selection of all breeding stock.
The disease usually occurs during periods of rapid growth.
Therefore, it has been suggested that nutrition that creates rapid
growth may lead to the increase in incidence of the disease. It has
been recommended that animals that are susceptible to the disease be
fed a diet that is lower in protein and fat, or that they are fed in a
limited manner to allow steady even growth during the first year of
Diet plays a major role in everything a dog
does or is. An over fed pup who is carrying more weight than optimum
has a greater statistical chance of developing OCD than a lean pup.
That is not to say that you should underfeed a growing pup just to
avoid skeletal deformities. That line of reasoning has been proven to
be in error. Rather, be certain to feed high quality meat-based diets
that do not have grain as their first ingredient. Diets with high
protein and fat seem to be a better choice for dogs and cats than those
diets high in carbohydrates like corn, wheat, soybean meal.
Treatment of OCD
Surgery is indicated in animals that show severe symptoms, in cases where large lesions are identified on radiographs, or when conservative treatments fail. The surgery is very straightforward. Usually the cartilage flap can be grasped with forceps and lifted away from the humerus. Some surgeons gently scrape the bed where the flap was situated in order to stimulate faster healing and some leave the area as it is. The joint is flushed again and closed with sutures. After surgery, rest for two weeks is recommended and then a gradual return to normal activity is encouraged. There is a very high success rate for surgery and most animals recover fully without any further problems.
Definition of a FractureA fracture is a break or crack in a bone. Although we commonly think of fractures as involving a leg, it is also possible to fracture other bones in one's body ex: the skull, jaw, spine, ribs, pelvis and as well as the long bones and small bones of the front and back limbs.
Practically every bone in your pet's body is susceptible to fracture, and some, like spinal fractures, have a higher priority to treat. The symptoms that arise with fractures are based on the body part injured and any organ damage. Fractures are usually caused by a traumatic event; however, pathologic fractures can occur from relatively low energy events when preexisting disease such as a tumor or a metabolic bone disease like arthritis weakens the bone.
Symptoms of a FractureThe symptoms that arise with fractures are based on the body part injured and any organ damage. Typical symptoms include:
Causes of FracturesA fracture is typically caused by some type of trauma to a bone. This trauma might occur as a result of a fall, physical abuse, motor vehicle accident, or disease. Normal, everyday activities can cause bone fractures in pets with diseases that weaken the bones.
Treatment of Fractures
Bone fractures should be treated as quickly as possible to avoid
complications and ensure complete healing. Regular exercise and
sufficient amounts of calcium in your pets diet help strengthen the
bones and prevent bone fractures. You can also help prevent bone
fractures and other skeletal-related injuries in your pet by limiting
the "playground" area of any dangerous objects.
Stress fractures often require no more than rest, anti-inflammatory medicines, and temporarily discontinuing the activity that has caused the injury.
More severe fractures, such as those that are open, multiple, or to the hip or back, need to evaluated right away. Most fractures are immobilized with a cast, brace, splint, or sling.
Surgery may be necessary when a fracture is open, severe, or has resulted in severe injury to the surrounding tissues. Severe fractures may require internal devices, such as screws, rods, or plates, to hold the bone in place. The length of time it takes for a bone fracture to heal and the need for physical therapy after treatment depend upon the severity of the fracture and the age and health of your pet.